| 小麦田麦家公对苯磺隆的抗性机理 |
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| 引用本文：王恒智,白霜,吴小虎,吴翠霞,刘伟堂,王金信.小麦田麦家公对苯磺隆的抗性机理.植物保护学报,2019,46(1):216-223 |
| DOI：10.13802/j.cnki.zwbhxb.2019.2017195 |
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| 中文摘要:为明确麦田阔叶杂草麦家公Lithospermum arvense L.对苯磺隆的抗性机理，以苯磺隆抗性和敏感型麦家公为材料，比较分析这2个生物型麦家公靶标酶乙酰乳酸合成酶（acetolactate synthase，ALS）、解毒酶谷胱甘肽-S-转移酶（glutathione-S-transferase，GST）以及保护酶过氧化物酶（peroxidase，POD）、超氧化物歧化酶（superoxide dismutase，SOD）和过氧化氢酶（catalase，CAT）对苯磺隆的响应差异性。结果表明，抗性麦家公ALS对苯磺隆的敏感性较敏感型麦家公显著下降，苯磺隆的抑制中浓度分别为0.187、0.036 μmol/L。苯磺隆胁迫后，抗性和敏感型麦家公ALS活性都出现下降，但抗性麦家公ALS活性可恢复，而敏感型麦家公ALS活性则不能恢复；2个生物型麦家公GST活性都能被苯磺隆诱导，但抗性麦家公GST累计活性为29.31 U，高于敏感型麦家公（25.90 U）；抗性麦家公SOD累计活性为24.49 U，较敏感型麦家公（19.31 U）高，且具有较强的恢复能力；抗性麦家公POD和CAT累计活性分别为126.92~550.68 U和41.41~77.19 U，也高于敏感型麦家公的93.75~271.04 U、42.17~57.28 U。因此，靶标酶ALS对苯磺隆敏感性减弱是麦家公产生抗性的一个重要原因，解毒酶GST、SOD、POD和CAT活性升高可能与抗性有关。 |
| 中文关键词:麦家公 乙酰乳酸合成酶 除草剂 苯磺隆 抗药性 |
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| Resistance mechanism of Lithospermum arvense L. to tribenuron-methyl in winter wheat field |
| Author Name | Affiliation | E-mail | | Wang Hengzhi | College of Plant Protection, Shandong Agricultural University, Tai'an 271018, Shandong Province, China | | | Bai Shuang | College of Plant Protection, Shandong Agricultural University, Tai'an 271018, Shandong Province, China | | | Wu Xiaohu | Institute of Plant Protection, Chinese Academy of Agricultural Sciences, Beijing 100193, China | | | Wu Cuixia | Tai'an Academy of Agricultural Sciences, Tai'an 271000, Shandong Province, China | | | Liu Weitang | College of Plant Protection, Shandong Agricultural University, Tai'an 271018, Shandong Province, China | liuwt@sdau.edu.cn | | Wang Jinxin | College of Plant Protection, Shandong Agricultural University, Tai'an 271018, Shandong Province, China | wangjx@sdau.edu.cn |
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| Abstract:To clarify the tribenuron-methyl-resistance mechanism in the broad-leaf weed Lithospermum arvense L. in wheat fields, the difference in the response of the target enzymes acetolactate synthase (ALS), metabolic enzyme glutathione-S-transferase (GST) and protective enzymes superoxide dismutase (SOD), peroxidase (POD), and catalase (CAT) to herbicides was analyzed by using tribenuronmethyl susceptible and resistant plants. The results showed that the in vitro ALS sensitivity to tribenuron-methyl was significantly reduced in resistant plants when compared with susceptible plants, and the IC50 values of tribenuron-methyl for ALS were 0.187 and 0.036 μmol/L for susceptible and resistant plants, respectively. In vivo experiments revealed that the ALS activity of resistant biotype could be recovered after temporarily inhibited by tribenuron-methyl treatment. However, the in vivo ALS activity of susceptible biotype was consistently reduced after tribenuron-methyl treatment. The GST activity could be induced by tribenuron-methyl treatment in all biotypes, while the resistant biotype had a greater accumulative activity (29.31 U) than the susceptible biotype (25.90 U). In addition, resistant plants had a higher SOD accumulative activity (24.49 U) and stronger recovery ability of SOD than that in sensitive plants (19.31 U); the resistant plants also hold higher POD activity (126.92-550.68 U), CAT activity (41.41-77.19 U) than those in susceptible plants (93.75-271.04 U, 42.17-57.28 U). Based on these findings, reduced ALS sensitivity to tribenuron-methyl was partly responsible for the tribenuronmethyl-resistance in L. arvense L., and the enhanced GST, SOD, POD, CAT activities might also contribute to the tribenuron-methyl resistance. |
| keywords:Lithospermum arvense L. acetolactate synthase (ALS) herbicide tribenuron-methyl resistance |
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